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Influence of intranasal and carotid cooling on cerebral temperature balance and oxygenation.

Nybo L, Wanscher M, Secher NH - Front Physiol (2014)

Bottom Line: Intranasal cooling induced a parallel drop in jugular venous and arterial blood temperatures by 0.30 ± 0.08°C (mean ± SD), whereas nasal ventilation and carotid cooling failed to lower the jugular venous blood temperature.Calculated cerebral capillary oxygen tension was 43 ± 3 mmHg at rest and remained unchanged during intranasal and carotid cooling, but decreased to 38 ± 2 mmHg (P < 0.05) following increased nasal ventilation.In conclusion, percutaneous cooling of the carotid arteries and intranasal cooling with balloon catheters are insufficient to influence cerebral oxygenation in normothermic subjects as the cooling rate is only 0.3°C per hour and neither intranasal nor carotid cooling is capable of inducing selective brain cooling.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutrition, Exercise and Sport Sciences, University of Copenhagen Copenhagen, Denmark.

ABSTRACT
The present study evaluated the influence of intranasal cooling with balloon catheters, increased nasal ventilation, or percutaneous cooling of the carotid arteries on cerebral temperature balance and oxygenation in six healthy male subjects. Aortic arch and internal jugular venous blood temperatures were measured to assess the cerebral heat balance and corresponding paired blood samples were obtained to evaluate cerebral metabolism and oxygenation at rest, following 60 min of intranasal cooling, 5 min of nasal ventilation, and 15 min with carotid cooling. Intranasal cooling induced a parallel drop in jugular venous and arterial blood temperatures by 0.30 ± 0.08°C (mean ± SD), whereas nasal ventilation and carotid cooling failed to lower the jugular venous blood temperature. The magnitude of the arterio-venous temperature difference across the brain remained unchanged at -0.33 ± 0.05°C following intranasal and carotid cooling, but increased to -0.44 ± 0.11°C (P < 0.05) following nasal ventilation. Calculated cerebral capillary oxygen tension was 43 ± 3 mmHg at rest and remained unchanged during intranasal and carotid cooling, but decreased to 38 ± 2 mmHg (P < 0.05) following increased nasal ventilation. In conclusion, percutaneous cooling of the carotid arteries and intranasal cooling with balloon catheters are insufficient to influence cerebral oxygenation in normothermic subjects as the cooling rate is only 0.3°C per hour and neither intranasal nor carotid cooling is capable of inducing selective brain cooling.

No MeSH data available.


Related in: MedlinePlus

Arterial, jugular venous and mean capillary oxygen tension (lower panel) and saturation (top panel) at rest (baseline), following 1 h of intranasal cooling, after 5 min of increased nasal ventilation and 15 min of carotid cooling. *Indicates that the value is different from corresponding value at rest (P < 0.05).
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Figure 3: Arterial, jugular venous and mean capillary oxygen tension (lower panel) and saturation (top panel) at rest (baseline), following 1 h of intranasal cooling, after 5 min of increased nasal ventilation and 15 min of carotid cooling. *Indicates that the value is different from corresponding value at rest (P < 0.05).

Mentions: MCA Vmean remained unchanged (within 2% of baseline values) during intranasal and carotid cooling, whereas it declined to 45 ± 7% of the baseline value at the end of the 5 min period with nasal ventilation. Accordingly, PaCO2 was similar at baseline (39.2 ± 0.7 mmHg) during intra-nasal (39.1 ± 0.9 mmHg) and carotid cooling (39.5 ± 0.9 mmHg), but declined to 20.9 ± 3.2 mmHg following 5 min of nasal ventilation. Furthermore, PaO2 and saturation were similar at baseline, following intranasal and carotid cooling (average PaO2 ~100 mmHg and saturation ~97.5%), but increased to 125.1 ± 3.7 mmHg and 99.6 ± 0.2% following the 5 min period with increased nasal ventilation (Figure 3). However, a-v DO2 increased from 83.5 ± 5.5 ml·l−1 at rest to 119.1 ± 7.0 ml·l−1 following the nasal ventilation period and the jugular venous and mean cerebral capillary oxygen tension were lowered by ~10 and 5 mmHg, respectively. In contrast, a-v DO2, jugular venous PO2 and mean cerebral capillary oxygen tension remained unchanged following intranasal and carotid cooling (Figure 3, lower panel). Also, a-vDglucose was similar at rest, following intranasal, and carotid cooling with an average of 0.55 ± 0.08 mmol·l−1 and the cerebral release of lactate remained low with an a-vDlactate of −0.05 ± 0.03 mmol·l−1. In contrast, a-vDglucose increased to 1.04 ± 0.16 mmol·l−1 and a-vDlactate was widened to −0.20 ± 0.07 mmol·l−1 following the period with nasal ventilation.


Influence of intranasal and carotid cooling on cerebral temperature balance and oxygenation.

Nybo L, Wanscher M, Secher NH - Front Physiol (2014)

Arterial, jugular venous and mean capillary oxygen tension (lower panel) and saturation (top panel) at rest (baseline), following 1 h of intranasal cooling, after 5 min of increased nasal ventilation and 15 min of carotid cooling. *Indicates that the value is different from corresponding value at rest (P < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3936139&req=5

Figure 3: Arterial, jugular venous and mean capillary oxygen tension (lower panel) and saturation (top panel) at rest (baseline), following 1 h of intranasal cooling, after 5 min of increased nasal ventilation and 15 min of carotid cooling. *Indicates that the value is different from corresponding value at rest (P < 0.05).
Mentions: MCA Vmean remained unchanged (within 2% of baseline values) during intranasal and carotid cooling, whereas it declined to 45 ± 7% of the baseline value at the end of the 5 min period with nasal ventilation. Accordingly, PaCO2 was similar at baseline (39.2 ± 0.7 mmHg) during intra-nasal (39.1 ± 0.9 mmHg) and carotid cooling (39.5 ± 0.9 mmHg), but declined to 20.9 ± 3.2 mmHg following 5 min of nasal ventilation. Furthermore, PaO2 and saturation were similar at baseline, following intranasal and carotid cooling (average PaO2 ~100 mmHg and saturation ~97.5%), but increased to 125.1 ± 3.7 mmHg and 99.6 ± 0.2% following the 5 min period with increased nasal ventilation (Figure 3). However, a-v DO2 increased from 83.5 ± 5.5 ml·l−1 at rest to 119.1 ± 7.0 ml·l−1 following the nasal ventilation period and the jugular venous and mean cerebral capillary oxygen tension were lowered by ~10 and 5 mmHg, respectively. In contrast, a-v DO2, jugular venous PO2 and mean cerebral capillary oxygen tension remained unchanged following intranasal and carotid cooling (Figure 3, lower panel). Also, a-vDglucose was similar at rest, following intranasal, and carotid cooling with an average of 0.55 ± 0.08 mmol·l−1 and the cerebral release of lactate remained low with an a-vDlactate of −0.05 ± 0.03 mmol·l−1. In contrast, a-vDglucose increased to 1.04 ± 0.16 mmol·l−1 and a-vDlactate was widened to −0.20 ± 0.07 mmol·l−1 following the period with nasal ventilation.

Bottom Line: Intranasal cooling induced a parallel drop in jugular venous and arterial blood temperatures by 0.30 ± 0.08°C (mean ± SD), whereas nasal ventilation and carotid cooling failed to lower the jugular venous blood temperature.Calculated cerebral capillary oxygen tension was 43 ± 3 mmHg at rest and remained unchanged during intranasal and carotid cooling, but decreased to 38 ± 2 mmHg (P < 0.05) following increased nasal ventilation.In conclusion, percutaneous cooling of the carotid arteries and intranasal cooling with balloon catheters are insufficient to influence cerebral oxygenation in normothermic subjects as the cooling rate is only 0.3°C per hour and neither intranasal nor carotid cooling is capable of inducing selective brain cooling.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutrition, Exercise and Sport Sciences, University of Copenhagen Copenhagen, Denmark.

ABSTRACT
The present study evaluated the influence of intranasal cooling with balloon catheters, increased nasal ventilation, or percutaneous cooling of the carotid arteries on cerebral temperature balance and oxygenation in six healthy male subjects. Aortic arch and internal jugular venous blood temperatures were measured to assess the cerebral heat balance and corresponding paired blood samples were obtained to evaluate cerebral metabolism and oxygenation at rest, following 60 min of intranasal cooling, 5 min of nasal ventilation, and 15 min with carotid cooling. Intranasal cooling induced a parallel drop in jugular venous and arterial blood temperatures by 0.30 ± 0.08°C (mean ± SD), whereas nasal ventilation and carotid cooling failed to lower the jugular venous blood temperature. The magnitude of the arterio-venous temperature difference across the brain remained unchanged at -0.33 ± 0.05°C following intranasal and carotid cooling, but increased to -0.44 ± 0.11°C (P < 0.05) following nasal ventilation. Calculated cerebral capillary oxygen tension was 43 ± 3 mmHg at rest and remained unchanged during intranasal and carotid cooling, but decreased to 38 ± 2 mmHg (P < 0.05) following increased nasal ventilation. In conclusion, percutaneous cooling of the carotid arteries and intranasal cooling with balloon catheters are insufficient to influence cerebral oxygenation in normothermic subjects as the cooling rate is only 0.3°C per hour and neither intranasal nor carotid cooling is capable of inducing selective brain cooling.

No MeSH data available.


Related in: MedlinePlus